First paragraph (this article has no abstract)

With great interest we read the recent article by Alfieri and colleagues [1], demonstrating that angiopoietin (Ang)-1 variant MAT.Ang-1 improved endotoxemiainduced
microvascular dysfunction and microvascular hyperpermeability. The authors suggested
that MAT. Ang-1-induced recovery of microcirculatory tissue perfusion during sepsis
is due to preservation of endothelial barrier integrity. To further elucidate the
mechanism, they investigated the possibility of involvement of VE-cadherin, a major
adherens junctions protein responsible for microvascular leakage in inflammation.
They found, however, while there was no change in overall expression of VE-cadherin,
MAT.Ang-1 increased VE-cadherin phosphorylation in the treated mice, which appears
unable to explain the observed endothelial barrier protective effects of MAT.Ang-1.